Discussion
It has been reported that hypertrophic cardiomyopathy or dilated
cardiomyopathy can cause AS.2,3 Some scholars have
proposed the AS is defined by: Atrial electrical activity could not be
recorded by routine ECG; The jugular pulse and wave disappeared; The
atrial contraction disappeared under X-ray fluoroscopy; QRS wave is the
supraventricular pattern; Higher intensity atrial stimulation does not
produce atrial excitement.4 Studies have found that
atrial muscle degeneration, necrosis, fibrosis, fat cell accumulation
and other pathological changes occurred in patients with AS and the
changes were mostly irreversible.5 Chhabra L et al.
reported that interatrial block will affect atrial electrical and
mechanical activity, especially the patients with left atrial
enlargement. The atrial injury leads to interatrial block, and finally
leads to atrial standstill.6 However, intracardiac
electrophysiological examination in AS has not been reported.
In this case, a small amount of potential was observed in the left
inferior pulmonary vein, and no electrical activity was measured in
other parts of the left atrium, which could indicate AS not caused by
interatrial block. AS caused by acute myocarditis has been
reported.7 Atrial nonpotential and AS after
pericardial effusion have been rarely reported. In this case,
rheumatism, tumor, tuberculosis and myocarditis were excluded according
to the examination. Pericardial effusion test suggested that
inflammatory cells increased, and pericardial effusion decreased after
anti-inflammatory treatment. However, the specific mechanism of AS was
unknown. The risk of thrombosis and stroke was significantly increased
in patients with AS and stroke has been reported in patients with
AS,8 so anticoagulation therapy should be actively
used in patients with AS. In this case, anticoagulation therapy was
performed and there may be other types of arrhythmia in the right atrium
during the follow-up.